Toll-like receptors are responsible for the recognition of most common patterns of bacterial and viral pathogens. Their activation results in recruitment of innate and subsequently adaptive immune response. Receptor cells of the immune system to the site of presence of antigens is the key step in effective immune response. That is why immunization involves the use of different types of adjuvants. Although the majority of tumors express tumor-specific antigens, they are using a number of mechanisms allowing then to escape immune recognition. It was recently demonstrated in mouse models that activation of TLR5 by its ligand and agonist, bacterial flagellin, results in the induction of antitumor effect against those tumors that express functional TLR5. This opens a general opportunity for considering TLR5 agonists for cancer immunotherapy. There are two major obstacles on the way to reduction of this idea to practice. First, is the rare incidence of tumors expressing functional TLR5 limiting applicability of this approach to only a small subset of tumors. Second, systemic administration of TLR5 agonist leads to activation of TRL5 signaling in all cells that have functional receptor making response unfocused and not tumor-specific. Accordingly, there is a need in the art for a mechanism or method for autocrine activation of TLR receptor signaling in infected or tumor cells with minimal systemic effect thus enabling to attract innate immune response specifically to the infected cell or tumor.